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Cancer Cell, ISSN 1535-6108, 2007, Volume 11, Issue 2, pp. 175 - 189
In response to DNA damage, eukaryotic cells activate ATM-Chk2 and/or ATR-Chk1 to arrest the cell cycle and initiate DNA repair. We show that, in the absence of... 
SIGNALING | CANCER-CELLS | ONCOLOGY | 7-HYDROXYSTAUROSPORINE UCN-01 | MITOTIC CATASTROPHE | SECKEL-SYNDROME | MAPKAP KINASE-2 | NUCLEAR EXPORT | INDUCED CYTOTOXICITY | 14-3-3 PROTEIN-BINDING | RADIOSENSITIZING AGENT | PHOSPHORYLATION SITES | Protein Kinases - genetics | Antibiotics, Antineoplastic - pharmacology | Humans | DNA Repair - radiation effects | Staurosporine - analogs & derivatives | Bone Neoplasms - pathology | G2 Phase - drug effects | Bone Neoplasms - metabolism | DNA-Binding Proteins - metabolism | Neoplasms, Experimental - pathology | Tumor Suppressor Protein p53 - physiology | Ultraviolet Rays | Antineoplastic Agents - pharmacology | p38 Mitogen-Activated Protein Kinases - metabolism | Phosphorylation - drug effects | cdc25 Phosphatases - metabolism | Osteosarcoma - metabolism | Protein-Serine-Threonine Kinases - metabolism | DNA Damage - drug effects | DNA Repair - drug effects | Tumor Suppressor Proteins - metabolism | Mitosis - radiation effects | G2 Phase - radiation effects | Signal Transduction | Cell Survival | Cell Cycle Proteins - metabolism | Cells, Cultured | Cell Division - radiation effects | Intracellular Signaling Peptides and Proteins | Protein Kinase C - antagonists & inhibitors | Ataxia Telangiectasia Mutated Proteins | Cisplatin - pharmacology | Cell Division - drug effects | Mice, Knockout | Phosphorylation - radiation effects | S Phase - radiation effects | Animals | Mitosis - drug effects | Mice, Nude | Protein Kinases - physiology | Mice | S Phase - drug effects | Neoplasms, Experimental - metabolism | DNA Damage - radiation effects | Doxorubicin - pharmacology | Osteosarcoma - pathology | Staurosporine - pharmacology | DNA
Journal Article
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 12/2011, Volume 108, Issue 50, pp. 20119 - 20124
Natural killer cell lymphoma (NKCL) constitutes a rare and aggressive form of non-Hodgkin lymphoma, and there is little insight into its pathogenesis. Here we... 
B lymphocytes | T cell lymphoma | B cell lymphoma | Cell lines | Cell cycle | Tumor suppressor genes | Natural killer cells | Methylation | Tumors | Apoptosis | Neoplastic transformation | NK-cell activation and homeostasis | Biotage pyrosequencing | CCNG2 | CCNG1 | PERIPHERAL T | LYMPHOMA/LEUKEMIA | biotage pyrosequencing | MULTIDISCIPLINARY SCIENCES | neoplastic transformation | TRANSCRIPTIONAL REPRESSOR BLIMP-1 | T-CELL | IDENTIFICATION | CONSISTENT PATTERNS | LYMPHOMA | DIFFERENTIATION | COMPARATIVE GENOMIC HYBRIDIZATION | LYMPHOCYTES | G2 Phase - genetics | Gene Silencing - drug effects | Apoptosis - drug effects | Humans | Killer Cells, Natural - pathology | Promoter Regions, Genetic - genetics | G2 Phase - drug effects | Lymphoma, Non-Hodgkin - pathology | Gene Knockdown Techniques | Time Factors | DNA Mutational Analysis | Tumor Suppressor Proteins - genetics | DNA Copy Number Variations - drug effects | Gene Expression Regulation, Neoplastic - drug effects | Repressor Proteins - metabolism | Cell Division - genetics | Interleukin-2 - metabolism | Tumor Suppressor Proteins - metabolism | Transduction, Genetic | Repressor Proteins - genetics | DNA Copy Number Variations - genetics | DNA Methylation - genetics | Lymphoma, Non-Hodgkin - genetics | Cell Division - drug effects | Biopsy | Culture Media - pharmacology | Interleukin-2 - pharmacology | Killer Cells, Natural - drug effects | Killer Cells, Natural - metabolism | DNA Methylation - drug effects | Positive Regulatory Domain I-Binding Factor 1 | RNA, Small Interfering - metabolism | Development and progression | Killer cells | Genetic aspects | Non-Hodgkin's lymphomas | Health aspects | Life Sciences | Biochemistry, Molecular Biology | Biological Sciences
Journal Article
Cancer Research, ISSN 0008-5472, 06/2010, Volume 70, Issue 12, pp. 4972 - 4981
The median survival for patients with locally advanced pancreatic cancer treated with gemcitabine and radiation is approximately 1 year. To develop improved... 
Protein Kinases - metabolism | Gamma Rays | Adenocarcinoma - pathology | Pancreatic Neoplasms - metabolism | Humans | DNA Repair - radiation effects | Protein Kinases - chemistry | Deoxycytidine - pharmacology | Immunoblotting | RNA, Messenger - metabolism | G2 Phase - drug effects | Immunoenzyme Techniques | Adenocarcinoma - metabolism | Flow Cytometry | Urea - analogs & derivatives | Protein-Serine-Threonine Kinases - antagonists & inhibitors | Drug Therapy, Combination | DNA Damage - drug effects | Rad51 Recombinase - metabolism | DNA Repair - drug effects | G2 Phase - radiation effects | Pancreatic Neoplasms - pathology | RNA, Messenger - genetics | Radiation-Sensitizing Agents - pharmacology | Pancreatic Neoplasms - radiotherapy | Thiophenes - pharmacology | Mice, SCID | Reverse Transcriptase Polymerase Chain Reaction | Adenocarcinoma - drug therapy | Blotting, Western | Xenograft Model Antitumor Assays | Animals | Fluorescent Antibody Technique | Cell Line, Tumor | Checkpoint Kinase 2 | Checkpoint Kinase 1 | Mice, Inbred NOD | Mice | Protein Kinase Inhibitors - pharmacology | Recombination, Genetic - radiation effects | DNA Damage - radiation effects | Deoxycytidine - analogs & derivatives | Recombination, Genetic - drug effects | Urea - pharmacology | pancreatic cancer | gemcitabine | Chk1 | radiosensitization | homologous recombination repair
Journal Article
European Journal of Nutrition, ISSN 1436-6207, 4/2014, Volume 53, Issue 3, pp. 853 - 864
Urolithins, gut microbiota metabolites derived from ellagic acid and ellagitannins, reach micromolar concentrations in the colon lumen where can have... 
Chemistry | Colon cancer | Nutrition | Urolithins | Phase-II metabolism | Ellagic acid | Cell cycle | Glucuronide | ELLAGITANNIN METABOLITES | MICROFLORA | INDUCED INFLAMMATION | MICROBIOTA | IN-VITRO | NUTRITION & DIETETICS | MOLECULAR MARKERS | RESISTANCE | ACID-DERIVED METABOLITES | CACO-2 CELLS | Coumarins - metabolism | Intestinal Mucosa - metabolism | Antibiotics, Antineoplastic - pharmacology | Colonic Neoplasms - drug therapy | Humans | Colon - drug effects | Anti-Inflammatory Agents, Non-Steroidal - chemistry | Coumarins - chemistry | Coumarins - antagonists & inhibitors | Colonic Neoplasms - metabolism | G2 Phase - drug effects | Intestinal Mucosa - drug effects | Anti-Inflammatory Agents, Non-Steroidal - pharmacology | Hydrolyzable Tannins - antagonists & inhibitors | Anti-Inflammatory Agents, Non-Steroidal - antagonists & inhibitors | Glucuronides - metabolism | Antibiotics, Antineoplastic - chemistry | Hydrolyzable Tannins - chemistry | Membrane Transport Modulators - pharmacology | ATP-Binding Cassette Transporters - metabolism | Hydrolyzable Tannins - pharmacology | Anti-Inflammatory Agents, Non-Steroidal - metabolism | Glucuronides - chemistry | Cell Survival - drug effects | Metabolic Detoxication, Phase II | Hydrolyzable Tannins - metabolism | Colon - metabolism | Coumarins - pharmacology | Cell Line, Tumor | Cell Proliferation - drug effects | S Phase - drug effects | Kinetics | Antibiotics, Antineoplastic - metabolism | ATP-Binding Cassette Transporters - antagonists & inhibitors | Drug Resistance, Neoplasm - drug effects | Metabolites
Journal Article
Cell, ISSN 0092-8674, 2002, Volume 109, Issue 4, pp. 459 - 472
Fanconi anemia (FA) and ataxia telangiectasia (AT) are clinically distinct autosomal recessive disorders characterized by spontaneous chromosome breakage and... 
TARGETED DISRUPTION | CHECKPOINT PATHWAY | DNA-DAMAGE RESPONSE | BIOCHEMISTRY & MOLECULAR BIOLOGY | S-PHASE | ATM-DEPENDENT PHOSPHORYLATION | NUCLEAR-COMPLEX | NIJMEGEN-BREAKAGE-SYNDROME | IONIZING-RADIATION | X-IRRADIATION | MAMMALIAN-CELLS | CELL BIOLOGY | Nucleic Acid Synthesis Inhibitors - pharmacology | Fanconi Anemia - metabolism | Humans | Ubiquitin - metabolism | Phosphoserine - antagonists & inhibitors | G1 Phase - drug effects | G2 Phase - drug effects | Genes, cdc - radiation effects | Cell Nucleus - metabolism | Cell Nucleus - radiation effects | Nuclear Proteins - deficiency | Fanconi Anemia - genetics | Signal Transduction - radiation effects | Nuclear Proteins - genetics | Protein-Serine-Threonine Kinases - metabolism | DNA-Binding Proteins | Radiation, Ionizing | Ataxia Telangiectasia - physiopathology | Fanconi Anemia Complementation Group D2 Protein | G2 Phase - radiation effects | Mutation - radiation effects | Protein-Serine-Threonine Kinases - genetics | Genes, cdc - drug effects | Ataxia Telangiectasia - metabolism | Signal Transduction - genetics | Ubiquitin - genetics | Ataxia Telangiectasia Mutated Proteins | Phosphoserine - metabolism | S Phase - genetics | Mitomycin - pharmacology | Phosphorylation - radiation effects | S Phase - radiation effects | Mutation - drug effects | G1 Phase - radiation effects | Signal Transduction - drug effects | Fanconi Anemia - physiopathology | Ataxia Telangiectasia - genetics | S Phase - drug effects | HeLa Cells | Cell Nucleus - drug effects | Cell Cycle Proteins | Cell Line, Transformed | Tumor Suppressor Proteins | Cell research | Ionizing radiation | Mitomycin | Analysis | Causes of | Physiological aspects | Ataxia telangiectasia | Genetic aspects | Gene expression | Chromosomes | Cells | Fanconi's anemia
Journal Article
Journal Article
DNA Repair, ISSN 1568-7864, 02/2014, Volume 14, Issue 1, pp. 27 - 38
Ultraviolet (UV)-induced DNA damage are removed by nucleotide excision repair (NER) or can be tolerated by specialized translesion synthesis (TLS) polymerases,... 
Cell cycle progression | Replication fork | UV damage bypass | γH2AX | TLS DNA polymerase η | NER | DNA strand breaks | UV-IRRADIATION | TLS DNA polymerase eta | TRANSLESION SYNTHESIS | DOUBLE-STRAND BREAKS | MAMMALIAN-CELLS | POLYMERASE ETA | NUCLEOTIDE EXCISION-REPAIR | HISTONE H2AX PHOSPHORYLATION | XERODERMA-PIGMENTOSUM | gamma H2AX | GENETICS & HEREDITY | CELL-CYCLE | TOXICOLOGY | CHECKPOINT ACTIVATION | G2 Phase - genetics | Genome, Human - radiation effects | DNA Replication - drug effects | Humans | DNA Repair - radiation effects | DNA-Directed DNA Polymerase - deficiency | Genome, Human - drug effects | DNA-Binding Proteins - deficiency | G2 Phase - drug effects | DNA Breaks, Double-Stranded - radiation effects | DNA, Single-Stranded - genetics | DNA Breaks, Single-Stranded - drug effects | Phosphorylation - genetics | DNA Breaks, Double-Stranded - drug effects | DNA Replication - radiation effects | Caffeine - pharmacology | Cell Cycle Checkpoints - genetics | Phosphorylation - drug effects | Cell Line | DNA Repair - drug effects | G2 Phase - radiation effects | DNA Breaks, Single-Stranded - radiation effects | DNA, Single-Stranded - metabolism | S Phase - genetics | Genome, Human - genetics | Ultraviolet Rays - adverse effects | DNA, Single-Stranded - biosynthesis | Phosphorylation - radiation effects | S Phase - radiation effects | Cell Cycle Checkpoints - radiation effects | Cell Cycle Checkpoints - drug effects | DNA Replication - genetics | S Phase - drug effects | DNA Damage | Histones - metabolism | Dose-Response Relationship, Radiation | Proteins | DNA damage | Genomics | DNA
Journal Article
The EMBO Journal, ISSN 0261-4189, 12/2006, Volume 25, Issue 24, pp. 5775 - 5782
The phosphatidyl inositol 3‐kinase‐like kinases (PIKKs), ataxia‐telangiectasia mutated (ATM) and ATM‐ and Rad3‐related (ATR) regulate parallel damage response... 
ataxia telangiectasia‐mutated protein | PIKKs | phosphorylation | DNA damage responses | Phosphorylation | Ataxia telangiectasia-mutated protein | RECRUITMENT | BIOCHEMISTRY & MOLECULAR BIOLOGY | ataxia telangiectasia-mutated protein | DNA-DAMAGE | COMPLEXES | PROTEIN-KINASES | CELL BIOLOGY | CHK1 | SECKEL-SYNDROME | CHECKPOINT | IONIZING-RADIATION | ATAXIA-TELANGIECTASIA | BINDING | Protein Kinases - metabolism | Hydroxyurea - pharmacology | Protein-Serine-Threonine Kinases - deficiency | DNA Replication - drug effects | Humans | G2 Phase - drug effects | DNA-Binding Proteins - metabolism | Ultraviolet Rays | DNA Replication - radiation effects | Phosphorylation - drug effects | Protein-Serine-Threonine Kinases - metabolism | Protein Structure, Tertiary | Tumor Suppressor Proteins - metabolism | Mitosis - radiation effects | G2 Phase - radiation effects | Cell Cycle Proteins - metabolism | Nuclear Proteins - metabolism | Ataxia Telangiectasia Mutated Proteins | Enzyme Activation - drug effects | Fibroblasts - pathology | Phosphoserine - metabolism | Enzyme Activation - radiation effects | Histones - deficiency | Phosphorylation - radiation effects | Animals | Mitosis - drug effects | Fibroblasts - radiation effects | Models, Biological | Fibroblasts - drug effects | Phosphoproteins - deficiency | Checkpoint Kinase 2 | Checkpoint Kinase 1 | Fibroblasts - cytology | Mice | Ions | Ultraviolet radiation | Molecular biology | Kinases | DNA damage
Journal Article